BACKGROUND AND AIMS: Inflammatory bowel diseases (IBD) have been reported to be caused by a complex interplay of immunological, infectious, and genetic factors. Previous studies have suggested that adipokines play a role in IBD by inducing proinflammatory cytokines. We aimed to evaluate the role of visfatin in the diagnosis algorithm of active IBD. METHODS: 85 newly diagnosed IBD patients [56 diagnosed with ulcerative colitis (UC) and 29 with Crohn's disease (CD)] and 30 healthy controls were included. IBD phenotypes were described accordingly to Montreal classification. Hemoglobin, total leucocytic count (TLC), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), albumin, fecal calprotectin and serum visfatin were measured. RESULTS: The serum visfatin level was found to be significantly higher in patients with IBD than those in the control group (p<0.001). It was significantly positively correlated with CRP, ESR, and FC in both IBD groups. Receiver operating characteristic curve analysis of visfatin in diagnosis of UC revealed an area under curve of 0.911. At cutoff ≥1.4 ng/ml, the sensitivity was 92.9% and the specificity was 86.7%.. In CD group, at the same cutoff, AUC was 0.974, sensitivity was 96.6% and specificity was 86.7%. There was a statistically significant elevation of serum visfatin in extensive UC (E3) as compared to the other groups. A cutoff ≥3.25 ng/ml revealed 88.9% sensitivity, and 100% specificity in detection of E3 UC. Serum visfatin was significantly increased in CD stricturing phenotype (B2) as compared to non-stricturing non-penetrating CD (B1). A cutoff ≥3.5 ng/ml revealed 83.3% sensitivity, and 100% specificity in detection of B2. CONCLUSIONS: The serum visfatin level were significantly higher in patients with IBD than in controls. Serum visfatin might be a novel noninvasive marker to detect activity in IBD patients and can be used as predictor of disease extension in patients with UC.
BACKGROUND AND AIMS: Inflammatory bowel diseases (IBD) have been reported to be caused by a complex interplay of immunological, infectious, and genetic factors. Previous studies have suggested that adipokines play a role in IBD by inducing proinflammatory cytokines. We aimed to evaluate the role of visfatin in the diagnosis algorithm of active IBD. METHODS: 85 newly diagnosed IBD patients [56 diagnosed with ulcerative colitis (UC) and 29 with Crohn's disease (CD)] and 30 healthy controls were included. IBD phenotypes were described accordingly to Montreal classification. Hemoglobin, total leucocytic count (TLC), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), albumin, fecal calprotectin and serum visfatin were measured. RESULTS: The serum visfatin level was found to be significantly higher in patients with IBD than those in the control group (p<0.001). It was significantly positively correlated with CRP, ESR, and FC in both IBD groups. Receiver operating characteristic curve analysis of visfatin in diagnosis of UC revealed an area under curve of 0.911. At cutoff ≥1.4 ng/ml, the sensitivity was 92.9% and the specificity was 86.7%.. In CD group, at the same cutoff, AUC was 0.974, sensitivity was 96.6% and specificity was 86.7%. There was a statistically significant elevation of serum visfatin in extensive UC (E3) as compared to the other groups. A cutoff ≥3.25 ng/ml revealed 88.9% sensitivity, and 100% specificity in detection of E3 UC. Serum visfatin was significantly increased in CD stricturing phenotype (B2) as compared to non-stricturing non-penetrating CD (B1). A cutoff ≥3.5 ng/ml revealed 83.3% sensitivity, and 100% specificity in detection of B2. CONCLUSIONS: The serum visfatin level were significantly higher in patients with IBD than in controls. Serum visfatin might be a novel noninvasive marker to detect activity in IBD patients and can be used as predictor of disease extension in patients with UC.